ArticleCommunications biology2023
Deletion of the autism-related gene Chd8 alters activity-dependent transcriptional responses in mouse postmitotic neurons.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Homozygous CHD8 mutation intensifies ASD phenotypes and attenuates sex differences.Molecular psychiatry · 2026Article
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.Genetics · 2025Article
- Gut microbiota and urine metabolomics signature in autism spectrum disorder children from Southern China.BMC pediatrics · 2025Article
- Persistent cortical excitatory neuron dysregulation in adultResearch square · 2025Article
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.bioRxiv : the preprint server for biology · 2025Article
- Duplication of the autism-related gene Chd8 leads to behavioral hyperactivity and neurodevelopmental defects in mice.Nature communications · 2025Article
- Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8.Cellular & molecular biology letters · 2025Article
- Identification and experimental validation of common genes associated with both pulmonary arterial hypertension and major depressive disorder.Frontiers in psychiatry · 2025Article
- The Deficiency of the ASD-Related Gene CHD8 Disrupts Behavioral Patterns and Inhibits Hippocampal Neurogenesis in Mice.Journal of molecular neuroscience : MN · 2024Article
- Neurodevelopmental functions of CHD8: new insights and questions.Biochemical Society transactions · 2024Review
- A bibliometric analysis of autism spectrum disorder signaling pathways research in the past decade.Frontiers in psychiatry · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CHD8 encodes chromodomain helicase DNA-binding protein 8 and its mutation is a highly penetrant risk factor for autism spectrum disorder (ASD). CHD8 serves as a key transcriptional regulator on the basis of its chromatin-remodeling activity and thereby controls the proliferation and differentiation of neural progenitor cells. However, the function of CHD8 in postmitotic neurons and the adult brain has remained unclear. Here we show that Chd8 homozygous deletion in mouse postmitotic neurons results in downregulation of the expression of neuronal genes as well as alters the expression of activity-dependent genes induced by KCl-mediated neuronal depolarization. Furthermore, homozygous ablation of CHD8 in adult mice was associated with attenuation of activity-dependent transcriptional responses in the hippocampus to kainic acid-induced seizures. Our findings implicate CHD8 in transcriptional regulation in postmitotic neurons and the adult brain, and they suggest that disruption of this function might contribute to ASD pathogenesis associated with CHD8 haploinsufficiency.
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